The ways in which plasmids inhibit the multiplication of bacteriophage are being investigated. It has been shown that during the Colicin Ib plasmid inhibition of T5 phage, cell membrane depolarization occurs. This leads to a loss of transport ability and macromolecular syntheses, causing the infection to be abortive. As the colicin protein itself can cause membrane depolarization it has been suggested that this protein may be involved in the abortive infection. To study the plasmid genes involved, and to see if, indeed, the colicin is responsible for the abortive infection, restriction fragments of the plasmid are being cloned into a pBR322 vector. Clones containing the colicin gene will be studied with respect to their immunity to the colicin protein and their ability to inhibit phage growth. Other clones with the ability to inhibit phage growth will also be studied in order to determine the relationship of all the genes involved in the abortive infection. Experiments to specifically mutate the Colicin Ib plasmid with Tn5, a kanamycin resistance transposon, are also underway. The mechanism by which R-plasmids inhibit phage multiplication in Salmonella is also being studied to see if there is a common mechanism for the many examples of abortive infection reported in the literature. Studies on membrane protein biosynthesis after phage infection are continuing.